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α7-Nicotinic Acetylcholine Receptor Activation Modulates BV2 Microglial Plasticity via miR-21/TNF-α/NFκB in Oxygen-Glucose Deprivation/Reoxygenation.
J Mol Neurosci
December 2024
Centre for Drug and Herbal Development, Faculty of Pharmacy, Universiti Kebangsaan Malaysia, Jalan Raja Muda Abdul Aziz, 50300, Kuala Lumpur, Malaysia.
Elevated inflammatory reactions are a significant component in cerebral ischemia-reperfusion injury (CIRI). Activation of α7-Nicotinic Acetylcholine Receptor (α7nAChR) reduces stroke-induced inflammation in rats, but the anti-inflammatory pathway in microglia under CIRI condition remains unclear. This study employed qRT-PCR, protein assays, NanoString analysis, and bioinformatics to examine the effects of PNU282987 treatment (α7nAChR agonist) on BV2 microglial functional differentiation in oxygen-glucose deprivation/reoxygenation (OGDR) condition.
View Article and Find Full Text PDFRationally Engineering Pro-Proteins and Membrane-Penetrating α‑Helical Polypeptides for Genome Editing Toward Choroidal Neovascularization Treatment.
Adv Mater
December 2024
Department of Thoracic Surgery, The Second Affiliated Hospital of Soochow University, Suzhou, 215004, China.
Ribonucleoprotein (RNP)-based CRISPR/Cas9 genome editing holds great potential for the treatment of choroidal neovascularization (CNV), which however, is challenged by the lack of efficient cytosolic protein delivery tools. Herein, reversibly-phosphorylated pro-proteins (P-proteins) with conjugated adenosine triphosphate (ATP) tags are engineered and coupled with a membrane-penetrating, guanidine-enriched, α-helical polypeptide (GP) to mediate robust and universal cytosolic delivery. GP forms salt-stable nanocomplexes (NCs) with P-proteins via electrostatic interaction and salt bridging, and the helix-assisted, strong membrane activities of GP enabled efficient cellular internalization and endolysosomal escape of NCs.
View Article and Find Full Text PDFWhere are we in targeting hypoxia-induced pathways in inflammatory arthritis? Current understanding, insights, and future directions.
Int Immunopharmacol
December 2024
Department of Medicine, Division of Rheumatology, Queen's University, Kingston, Ontario, Canada; Faculty of Health Sciences, School of Medicine, Queen's University, Kingston, Ontario, Canada; Translational Institute of Medicine, Department of Medicine, Queen's University, Ontario, Canada; Rheumatology Clinic, Kingston Health Science Centre, Kingston, Ontario, Canada. Electronic address:
Introduction: Joint tissues affected by inflammatory arthritis (IA) create hypoxic microenvironments that sustain the inflammatory response. Although targeting molecules in hypoxia-induced pathways has provided valuable insights into potential novel therapies for various types of IA, progress remains preclinical, and no clinical trials have been conducted for IA.
Methods: A literature search was conducted to create a narrative review exploring the role of hypoxia and its signaling pathways in IA pathogenesis, as well as the potential and future directions for IA therapies that target hypoxia-induced molecules before moving forward to clinical applications.
Sevoflurane Alleviates Myocardial Ischemia/Reperfusion Injury by Targeting the circ_CDR1as/miR-671-5p/HMGA1 Axis.
J Biochem Mol Toxicol
January 2025
Intensive Care Unit, The Third Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, China.
Sevoflurane (Sev) has a cardioprotective role in myocardial ischemia/reperfusion injury (MI/RI), but its mechanism has not been fully elucidated. This study aimed to investigate whether the circ_CDR1as/miR-671-5p/HMGA1 axis mediates the cardioprotective effect of Sev in MI/RI. Cardiomyocytes underwent hypoxia/reoxygenation (H/R) treatment was used to simulate MI/RI in vitro.
View Article and Find Full Text PDFUnderstanding the development of tuberculous granulomas: insights into host protection and pathogenesis, a review in humans and animals.
Front Immunol
December 2024
Department of Academic Affairs, National Jewish Health, Denver, CO, United States.
Granulomas, organized aggregates of immune cells which form in response to (), are characteristic but not exclusive of tuberculosis (TB). Despite existing investigations on TB granulomas, the determinants that differentiate host-protective granulomas from granulomas that contribute to TB pathogenesis are often disputed. Thus, the goal of this narrative review is to help clarify the existing literature on such determinants.
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